FLT3 and cancer: In contrast, mutations of Aspβ9, which occupies a central position on the activation loop and is highly mutated in cancer (e.g. KIT D816V, PDGFRA D842V, FLT3 D835Y, position 7 in Figure 4), comprised one of the top mutation clusters, providing proof of principle that structural areas of high mutational burden across kinases harbor oncogenic mutations.